This article from the National Institutes of Health (NIH) takes a look at some of the mainstream research efforts aimed at measuring and better understanding the processes of biological aging. Where intervention arises from this part of the field, efforts tend to focus on altering the operation of metabolism to modestly slow aging, such as via the use of autophagy-promoting drugs like rapamycin and other mTOR inhibitors. The alternative, much better approach of identifying and repairing specific forms of cell and tissue damage in order to produce rejuvenation, continues to receive less attention, despite the compelling data produced by senolytic drugs that clear senescent cells.
With advancing age comes an increased risk of disease and disability. As people live longer, they are more likely to develop at least one age-related disease. Aging in people results from the gradual accumulation of defects and damage to the molecules and cells that make up our bodies. Unlike a car, our bodies have built-in mechanisms for repairing this damage. But even these repair mechanisms wear out over time. Eventually, enough damage accumulates to affect the function of whole organs and systems. NIH-funded researchers have been working to better understand aging at the molecular level. They're studying ways to measure differences in how people age before health problems appear. They're also exploring possible ways to slow, or even reverse, aging at the molecular level. This could lead to better approaches to prevent or treat age-related disease and disability.
Before you can tell if a treatment could slow or even reverse aging, you need to know how fast someone is aging in the first place. It's no secret that people age at different rates. Some people remain healthy and disease-free well into their ninth or even tenth decade of life. Others develop age-related diseases, such as cancer, heart disease, and dementia, much earlier. The concept of "biological age" is often used to describe these differences. Biological age reflects the molecular damage that accumulates over the years and eventually leads to disease and disability. Differences in biological age can develop years before age-related diseases appear. So a treatment to slow aging would also need to start well before such diseases appear. Then, to find out if a treatment worked or not, you'd have to track people for the rest of their lives. That's why researchers have been working to develop "aging clocks" to measure a person's biological age.
Age-reversing therapies like these are still some way in the future. Still, there are hints of lifestyle interventions that may have potential to lengthen life and delay aging. One that's been particularly well-studied is calorie restriction (CR). This is where you reduce the total number of calories you consume, but still get enough of the essential nutrients. To find out whether CR might have benefits in humans, too, NIH funded the Comprehensive Assessment of Long-Term Effects of Reducing Intake of Energy (CALERIE) study. More than 200 healthy, middle-aged volunteers were randomly assigned to two groups. Participants in one group were challenged to reduce their daily caloric intake by 25% for two years and given dietary and behavioral strategies for doing so. Those in the other group continued to eat their normal diets. Researchers examined the pace of biological aging in CALERIE participants. Those in the CR group had a much slower pace of aging as measured by clinical blood biomarkers. They also had a small but significant decrease in DunedinPACE, a rate of aging clock, while participants in the other group did not.
Link: https://www.nih.gov/news-events/nih-research-matters/research-context-can-we-slow-aging
View the full article at FightAging
